Uterine packing with chitosan-covered gauze for control of postpartum hemorrhage.

OBJECTIVE: To describe the use of gauze covered with chitosan, a potent hemostatic agent derived from chitin, in the treatment of postpartum hemorrhage (PPH). STUDY DESIGN: Patients suffering from postpartum hemorrhage were treated by uterine packing with chitosan-covered gauze, either through the hysterotomy in case of cesarean delivery or transvaginally, for up to 24 hours. RESULTS: Chitosan-covered gauze was used in 19 cases of postpartum hemorrhage due to uterine atony, placenta accreta/increta, or anticoagulation, including 5 severe cases where a hysterectomy seemed inevitable otherwise. In all but one case, the bleeding stopped and further interventions were avoided. Over comparable periods of time (18 months) and births (3822 vs 4077) before and after the introduction of the chitosan gauze in our clinic, the rate of peripartum hysterectomies was reduced by 75% (8 vs 2; odds ratio, 4.27; P = .044). CONCLUSION: Chitosan-covered gauze is a viable option in the treatment of (severe) postpartum hemorrhage. It is easy to use and requires no special training. It can be used after both vaginal and cesarean deliveries, and there are no adverse side effects. Furthermore, it is very inexpensive compared with other treatment options, making it suitable for use also in low resource-countries, where the death toll due to postpartum hemorrhage is especially high.

Postpartum hemorrhage: use of hemostatic combat gauze.

Cheap and simple interventions that are intended to minimize postpartum hemorrhage are of major public health concern. We report a case of postpartum hemorrhage in which conservative interventions had failed. The use of a chitosan-covered gauze that originally was developed for combat trauma allowed us to achieve hemostasis, and a seemingly inevitable hysterectomy was avoided.

Short-term administration of ethanol does not affect functional recovery from myocardial stunning in awake dogs.

UNLABELLED: Chronic ingestion of small doses of ethanol protects the myocardium from ischemic damage. It was demonstrated that short-term administration of ethanol (SAE) enhances the recovery of stunned myocardium in acutely instrumented, anesthetized dogs. It is unclear whether this beneficial effect of SAE also occurs in awake dogs. Therefore, we investigated the effects of SAE on regional myocardial stunning in awake dogs. Thirty-six dogs were chronically instrumented for measurement of heart rate, left atrial, aortic, and left ventricular pressure, left systolic ventricular contactility (dP/dt(max)) and diastolic ventricular function (dP/dt(min)), and regional myocardial wall-thickening fraction (WTF). Occluders around the left anterior descending (LAD) artery allowed the induction of reversible ischemia in the LAD-perfused myocardium. The dogs were assigned to one of three groups that differed in the dose of ethanol administered in the ethanol experiment (I, 0.125 g/kg [n = 12]; II, 0.25 g/kg [n = 12]; III, 0.5 g/kg [n = 12]). In each group, the dogs underwent two ischemic episodes (randomized crossover fashion; separate days): 10 min of LAD occlusion after the application of ethanol IV over 30 min (ethanol group) and without ethanol (control). WTF and hemodynamic variables were measured at baseline and at predetermined time points until complete recovery of myocardial stunning occurred. LAD-ischemia led to a significant decrease of LAD-WTF in all groups. There was no difference in WTF and hemodynamic variables with or without SAE during reperfusion. We conclude that SAE (0.125 g/kg, 0.25 g/kg, and 0.5 g/kg) does not significantly affect myocardial stunning in conscious dogs. IMPLICATIONS: In contrast to previous experiments in anesthetized dogs, short-term administration of ethanol does not alter myocardial stunning in conscious dogs.

Naloxone improves splanchnic perfusion in conscious dogs through effects on the central nervous system.

BACKGROUND: In patients undergoing colonoscopy, naloxone has vasodilative properties. However, it remains unclear whether this effect is mediated by central or peripheral mechanisms. The aim of this study was to investigate whether these effects are mediated by an effect of naloxone on the central nervous system. METHODS: Twenty dogs were chronically instrumented for measurement of hemodynamic parameters. Splanchnic blood flow was determined using colored microspheres. Transthoracic echocardiographic examinations were performed to measure cardiac output. In each animal, two experiments were performed in a random order: experiment 1 was determination of splanchnic blood flow before and 5 min after intravenous administration of naloxone (63 microg/kg), and experiment 2 was determination of splanchnic blood flow before and 5 min after administration of naloxone methiodide (63 microg/kg), which does not cross the blood-brain barrier. RESULTS: Naloxone, but not naloxone methiodide, significantly increased blood flow to the stomach (from 0.41 +/- 0.022 to 0.9 +/- 0.016# ml x g (-1) x min(-1) with naloxone), jejunum (from 0.31 +/- 0.024 to 0.83 +/- 0.083# ml x g(-1) x min(-1) with naloxone), colon (from 0.41 +/- 0.057 to 0.68 +/- 0.008# ml x g(-1) x min(-1) with naloxone), spleen (from 1.45 +/- 0.21 to 2.13 +/- 0.25# ml x g(-1) x min(-1) with naloxone), pancreas (from 0.97 +/- 0.021 to 1.25 +/- 0.005# ml x g(-1) x min(-1) with naloxone), and kidneys (from 3.24 +/- 0.108 to 5.31 +/- 0.26# ml x g(-1) x min(-1) with naloxone), without altering cardiac output or arterial blood pressure in conscious dogs. There were no differences in the hemodynamics or cardiac output between the two experiments. Data are presented as mean +/- SD. CONCLUSIONS: The increased splanchnic perfusion after naloxone is not caused by direct peripheral vascular effects or increased cardiac output. Indirect vasodilative effects on splanchnic vessels mediated by actions of naloxone on the central nervous system account for the increased gastrointestinal perfusion after naloxone in dogs.